Glucocorticoid-induced leucine zipper (GILZ) and serum/glucocorticoid-regulated kinase-1 (SGK-1) are key proteins induced by glucocorticoids. Recent research has highlighted that cortisol can be locally produced in the oral mucosa, potentially influencing the tissue expression of GILZ and SGK-1. Both proteins have been implicated in the pathogenesis of various cancers; however, their expression patterns in potentially malignant oral lesions, such as epithelial dysplasia, and in malignant lesions like squamous cell carcinoma (SCC) remain largely unexplored. This study aimed to investigate the hypothesis that the expression profiles of GILZ, SGK-1, and the phosphorylated (active) form of SGK-1 (pSGK-1) differ between epithelial dysplasia and SCC. To test this, archived paraffin-embedded biopsy samples underwent immunohistochemical analysis to determine tissue localization and expression of the target proteins. Histopathological evaluation using hematoxylin and eosin staining classified the samples into mild-to-moderate dysplasia, severe dysplasia, or SCC, with benign keratosis serving as a control. Immunohistochemistry revealed that all tissue types expressed SGK-1 and pSGK-1. SGK-1 was predominantly cytoplasmic, whereas pSGK-1 localized mainly to the cell membrane. In contrast, GILZ showed primarily nuclear staining across all samples. Semi-quantitative analysis indicated that GILZ expression was elevated in epithelial dysplasia but decreased in SCC to levels comparable to benign keratosis. Conversely, SGK-1 and pSGK-1 expression were reduced in SCC compared with benign keratosis or dysplastic tissues. Overall, although the immunostaining patterns of GILZ, SGK-1, and pSGK-1 did not clearly distinguish epithelial dysplasia from SCC, the differences in subcellular localization and expression suggest that these proteins may have distinct functional roles in dysplastic versus malignant oral lesions compared with benign keratosis.
